Periostin and sclerostin levels in individuals with spinal cord injury and their relationship with bone mass, bone turnover, fracture and osteoporosis status.

Abstract

Spinal cord injury (SCI) induces an acute alteration in bone metabolism. Although the aetiology of the bone disturbances is not precisely known, immobilisation reduces mechanical loading and the morphology of osteocytes, which are the primary mechanosensors. Periostin and sclerostin are secreted mostly by osteocytes and are involved in bone's mechanical response. The present study was conducted to determine whether individuals with SCI present alterations in serum periostin and sclerostin and to assess their relationships with bone mineral density, bone turnover markers, fracture status, time since injury, densitometric osteoporosis and paraplegic vs. tetraplegic status. One hundred and thirty-one individuals with SCI (96 males and 35 females; 42.8 ± 13.7 yr old) with a mean 14.2 ± 12.1 years since the time of injury were evaluated and compared with 40 able-bodied controls in a cross-sectional study. Periostin and sclerostin were assayed by ELISA from Biomedica® (Vienna, Austria), and bone turnover markers and areal bone mineral density (aBMD) were concomitantly analysed. Compared with controls, individuals with SCI presented higher periostin (p < 0.01), lower sclerostin (p < 0.001), similar markers of bone turnover levels and lower aBMD at the hip. Compared with chronic individuals, bone turnover markers, sclerostin excepted, values were higher as well as aBMD at hip in individuals with acute SCI. Moreover, the aBMD differences were more marked in tetraplegic than paraplegic individuals. Bone mineral density, fracture status, densitometric osteoporosis and paraplegia vs. tetraplegia did not seem to substantially influence the values of biological markers, sclerostin excepted. This study showed for the first time that individuals with SCI presented higher periostin levels than healthy controls only during the acute phase. Conversely, sclerostin levels are lower whatever the post-injury time. Fractures and densitometric osteoporosis were not associated with differences in these two biological markers, whereas paraplegia vs. tetraplegia and fragility fracture status seemed to influence sclerostin levels only.